Encouraging results were recently reported for midostaurin in a ‘real‐world’ setting, namely higher remission rates in midostaurin‐treated patients that translated into an increased rate of transplantation in first remission.41 These promising clinical responses, coupled with pre‐clinical and clinical studies suggesting efficacy of midostaurin in mutant FLT3 as well as non‐mutated FLT3‐expressing patients, strongly support the investigation of midostaurin as a therapeutic for a more general population of AML patients. This evidence concerns the gene FLT3 and acute myeloid leukemia.